Multiple Ca2+ channel types coexist to regulate synaptosomal neurotransmitter release.

Multiple Ca2+ channel types coexist to regulate synaptosomal neurotransmitter release.
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多种 Ca2 通道类型共存来调节突触体神经递质的释放。

DOI:
10.1073/pnas.90.20.9518
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发表时间:
1993
影响因子:
11.1
通讯作者:
Dunlap,K
Dunlap,K
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Turner,TJ;Adams,ME;Dunlap,K

文献摘要

被引文献

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Ca2+通道对兴奋-分泌耦合的调节是神经末梢的基本特性。阻断特定Ca2+通道类型的肽毒素已被用于确定哪些通道参与神经递质释放。对大鼠纹状体突触体释放的[3H]-谷氨酸和[3H]多巴胺的亚秒测量表明,对Agelenopsis aperta毒液肽- omega-Aga-IVA敏感的p型通道触发了这两种递质的释放。多巴胺(而不是谷氨酸)的释放也受n型ω -conotoxin敏感通道的控制。在强去极化的情况下,两种毒素单独使用都不是很有效,omega-Aga-IVA和omega- concontoxin联合使用可以协同抑制60-80%的Ca(2+)依赖性多巴胺释放。结果表明,在正常生理条件下,多种Ca2+通道类型共存,调节大多数神经末梢的神经分泌。P型和n型通道在多巴胺末端共存,而P型和抗ω - concontoxin和ω - aga - iva的通道在谷氨酸末端共存。这样的安排可以在不同的刺激和调制条件下对发射机释放的调节提供高度的灵活性。
The regulation of excitation-secretion coupling by Ca2+ channels is a fundamental property of the nerve terminal. Peptide toxins that block specific Ca2+ channel types have been used to identify which channels participate in neurotransmitter release. Subsecond measurements of [3H]-glutamate and [3H]dopamine release from rat striatal synaptosomes showed that P-type channels, which are sensitive to the Agelenopsis aperta venom peptide omega-Aga-IVA, trigger the release of both transmitters. Dopamine (but not glutamate) release was also controlled by N-type, omega-conotoxin-sensitive channels. With strong depolarizations, where neither toxin was very effective alone, a combination of omega-Aga-IVA and omega-conotoxin produced a synergistic inhibition of 60-80% of Ca(2+)-dependent dopamine release. The results suggest that multiple Ca2+ channel types coexist to regulate neurosecretion under normal physiological conditions in the majority of nerve terminals. P- and N-type channels coexist in dopaminergic terminals, while P-type and a omega-conotoxin- and omega-Aga-IVA-resistant channel coexist in glutamatergic terminals. Such an arrangement could lend a high degree of flexibility in the regulation of transmitter release under diverse conditions of stimulation and modulation.